Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMCOpen access

Type 2 Diabetes Modulates Mesenchymal Stem Cell Response to Advanced Glycation End Products and N-Acetylcysteine Antioxidant Effect

Landon R., Ding J., Bakari WN., Larochette N., El-Hafci H., Thibaudeau O.

Laboratory Study on Type 2 Diabetes, published in Pharmaceutics (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Laboratory Study
Journal
Pharmaceutics (2026)
Reported sample size
—
Source database
Europe PMC
PMID
42198289
PMCID
PMC13210573
DOI
10.3390/pharmaceutics18050595

Abstract (original English)

Background : Advanced glycation end products (AGEs) and oxidative stress (OS) have been linked to bone complications related to type 2 diabetes mellitus (T2DM). However, the effects of AGEs and OS on bone marrow mesenchymal stromal cells (BMMSCs), which play a key role in bone homeostasis and repair, remain unclear. Objectives : This study aimed to investigate the effects of AGEs on BMMSCs function and the ability of N-acetylcysteine (NAC) to alleviate AGE-induced OS in a T2DM context. Methods : Bone marrow (BM) and BMMSCs were isolated from Zucker diabetic fatty (ZDF) rats, which serve as a T2DM model, and their lean littermates (ZL, controls) at 24 weeks of age. Results : The results show that long-standing T2DM leads to changes in the BM's cellular composition and BMMSCs function that are distinct from age-related changes. In vitro, AGEs decreased BMMSCs viability, proliferation, and migration. The effects of AGEs were stronger in BMMSCs derived from a T2DM microenvironment. In both T2DM- and ZL-BMMSCs, AGEs induced cytoplasmic ROS, which was differentially reduced by NAC. The effect of NAC on T2DM-BMMSCs was greater when the cells were pre-treated with NAC 24 h before exposure to AGEs, whereas simultaneous exposure to both resulted in a smaller effect. Conclusions : These results show that AGEs impair BMMSCs expansion and functionality. AGE-induced ROS generation may be a c

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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